"Apoptosis (Programmed Cell Death) is a common phenomenon during development and used to eliminate harmful or unwanted cells from the organism. Apoptosis is the crucial process for organisms to keep their cellular homeostasis. It is known that deregulation of apoptosis is involved in many diseases, for instance, inefficient apoptosis has been found in many different cancers. Since all cells have the genetic machinery required to commit suicide, the ability to selectively regulate this process has profound implications for treating disease. Because more and more evidence indicates that irregular cell growth often leads to apoptosis, we believe that in addition to the promoting growth signals, inactivation of apoptosis is essential for normal cells to become tumor cells. This can be achieved by either increasing a signal that actively blocks apoptosis or generating a defective mutation in the cell death machinery. To identify these apoptosis-inactivating targets in different cancers will greatly enrich our knowledge about tumorigenesis and help to develop new cancer therapies. One of our research interests is to identify the targets that protect cancer cells from apoptosis, and, upon understanding the mechanisms of their actions, to develop new cancer therapies. To do so, we will use tumor necrosis factor (TNF)-mediated apoptosis as a model system. In previous study, we found that apoptosis, activation of transcription factor NF-kB, and the activation of c-Jun kinase JNK, three of the responses induced by TNF, are mediated by distinct pathways. We will focus on the anti-apoptotic effect mediated by the transcription factor NF-kB. The identification of the anti-apoptotic genes activated by NF-kB will provide new targets for improving TNF cancer therapeutic value. Reactivating apoptosis in cancer cells will be an important cancer therapy."